ReviewCureus2025
Causes, Diagnosis, Treatment, and Prognosis of Cardiac Fibrosis: A Systematic Review.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Mechanobiological feedback loops and quantitative decision thresholds in organ fibrosis: Translational principles for antifibrotic therapy.Journal of cell communication and signaling · 2026Review
- Galectin-3, transforming growth factor beta 1, and brain natriuretic peptide in cardiac remodeling under hyperlipidemic and hyperglycemic stress.Molecular and cellular biochemistry · 2026Article
- Review
- Serum Mucin-1 (CA15-3) in Relation to Pulse Pressure Amplification in Untreated Chinese Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2026Article
- Functional and Histological Analysis of Stem Cell and Amniotic Membrane Implantation After Acute Myocardial Infarction with Left Ventricular Dysfunction: Experimental Study.International journal of molecular sciences · 2026Article
- Versatile hiPSC Models and Bioengineering Platforms for Investigation of Atrial Fibrosis and Fibrillation.Cells · 2026Review
- Toward Precision in Myocardial Injury Management: A Critical Synthesis and the C.A.L.I.B.R.A.T.E. Framework for Biomarker Integration.Clinical Medicine Insights. Cardiology · 2026Review
- Beyond Organ-Specific Therapies: A Unified Approach to Multi-Organ Fibrosis.Drug design, development and therapy · 2026Review
- HDAC5 Inhibition as a Therapeutic Strategy for Titin Deficiency-Induced Cardiac Remodeling: Insights from Human iPSC Models.Medicines (Basel, Switzerland) · 2025Article
- Biomarkers in Heart Failure: A Review and a Wish.International journal of molecular sciences · 2025Review
- Longitudinal Myocardial Deformation as an Emerging Biomarker for Post-Traumatic Cardiac Dysfunction.Life (Basel, Switzerland) · 2025Review
- Cardiac magnetic resonance research advances in myocardial fibrosis of hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis, characterized by excessive extracellular matrix deposition, contributes to heart failure, arrhythmias, and myocardial dysfunction. Despite advances in understanding its mechanisms, targeted antifibrotic therapies remain limited. This review examines the causes, molecular mechanisms, diagnostic approaches, and therapeutic strategies for cardiac fibrosis. A systematic review of peer-reviewed studies was conducted, focusing on the etiology, diagnosis, treatment, and prognosis of cardiac fibrosis with no specific timeframe. The condition is driven by fibroblast activation, inflammatory pathways, and mechanical stress, with key contributing factors including ischemic heart disease, hypertension, diabetes, and aging. Diagnostic tools such as cardiac magnetic resonance imaging with T1 mapping and biomarkers play a crucial role, with natriuretic peptides offering both diagnostic and prognostic value. Galectin-3 has also shown promise as a prognostic marker. Current therapies, including RAAS inhibitors and beta-blockers, help prevent fibrosis progression but do not reverse established fibrosis. Emerging strategies such as plant-based compounds, gene therapy, fibroblast-targeting vaccines, and stem cell reprogramming show potential in preclinical studies. However, cardiac fibrosis remains a major driver of heart disease progression, and existing treatments remain limited. Major gaps include the lack of validated antifibrotic agents and challenges in translating preclinical findings into clinical applications. Further research is essential to develop effective targeted interventions.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.